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Munoz-Viana, R.

Publications and source records attributed to Munoz-Viana, R..

2 recordsLinked to original sources

Postembryonic developmental roles of the Arabidopsis KEULE gene

Cytokinesis in plant cells begins with the fusion of vesicles that transport cell wall materials at the center of the cell division plane, where the cell plate forms and expands radially until it fuses with the parental cell wall at the preprophase band. Vesicle fusion is facilitated by trans-SNARE complexes, with assistance from Sec1/Munc18 (SM) proteins. The SNARE protein KNOLLE and the SM protein KEULE are required for membrane fusion at the cell plate. Due to the crucial function of KEULE, all Arabidopsis (Arabidopsis thaliana) keule mutants identified to date are seedling lethal. Here, we identified the Arabidopsis serrata4-1 (sea4-1) and sea4-2 mutants, which carry recessive, hypomorphic alleles of KEULE. Homozygous sea4-1 and sea4-2 plants are viable and fertile but exhibit smaller rosettes and fewer leaves at bolting than the wild type. Their leaves are serrated, small, and undulated, with a complex venation pattern, develop necrotic patches, and undergo premature senescence. We established a likely relationship between these phenotypes and their defects in cytokinesis through reduced cell wall integrity and increased unfolded protein response. These findings shed light on the roles of KEULE in postembryonic development, particularly in the patterning of rosette leaves and leaf margins.

plant biology↗

Neuronal identity is maintained in the adult brain through KAT3-dependent enhancer acetylation

Very little is known about the mechanisms responsible for maintaining cell identity in mature tissues. The paralogous type 3 lysine acetyltransferases (KAT3) CBP and p300 are both essential during development, but their specific functions in nondividing differentiated cells remains unclear. Here, we show that when both proteins are simultaneously knocked-out in excitatory neurons of the adult brain, the mice express a rapidly progressing neurological phenotype associated with reduced dendritic complexity and electrical activity, the transcriptional shutdown of neuronal genes, and a dramatic loss of H3K27 acetylation and pro-neural transcription factor binding at neuronal enhancers. The neurons lacking both KAT3 rapidly acquire a molecularly undefined fate with no sign of dedifferentiation, transdifferentiation or death. Restoring CBP expression or lysine acetylation reestablished neuronal-specific transcription. Our experiments demonstrate that KAT3 proteins act as fate-keepers in excitatory neurons and other cell types by jointly safeguarding chromatin acetylation levels at cell type-specific enhancers throughout life.

cell biology↗